From the Guidelines
Drug-induced lupus (DIL) is an autoimmune disorder that mimics systemic lupus erythematosus but is triggered by certain medications. The most common drugs associated with DIL include hydralazine, procainamide, isoniazid, minocycline, and tumor necrosis factor (TNF) inhibitors. Symptoms typically include:
- Joint pain
- Muscle aches
- Fatigue
- Fever
- Skin rashes, though they are usually milder than in idiopathic lupus. The primary treatment for DIL is discontinuation of the offending medication, after which symptoms generally resolve within weeks to months. During recovery, symptomatic treatment may include NSAIDs for joint pain and antimalarials like hydroxychloroquine (200-400 mg daily) for skin manifestations and arthritis, as supported by the 2019 EULAR recommendations for the management of systemic lupus erythematosus 1. Corticosteroids are rarely needed but may be used for severe symptoms. Unlike idiopathic lupus, DIL rarely affects major organs like the kidneys or central nervous system. Laboratory findings typically show positive antinuclear antibodies (ANA) and anti-histone antibodies, with anti-dsDNA antibodies usually remaining negative. Patients with a history of DIL should avoid the triggering medication and related drugs in the future, and healthcare providers should be informed about this reaction to prevent recurrence. It is essential to note that the management of SLE, as outlined in the 2019 EULAR recommendations 1, focuses on achieving remission or low disease activity and preventing flares, which may also be applicable to the management of DIL. However, the primary goal in DIL is the discontinuation of the offending medication, which is not a consideration in idiopathic lupus.
From the FDA Drug Label
In a few patients hydrALAZINE may produce a clinical picture simulating systemic lupus erythematosus including glomerulonephritis. A lupus erythematosus-like syndrome of arthralgia, pleural or abdominal pain, and sometimes arthritis, pleural effusion, pericarditis, fever, chills, myalgia, and possibly related hematologic or skin lesions is fairly common after prolonged PA administration Positive ANA titers have been reported in patients receiving propafenone They have been reversible upon cessation of treatment and may disappear even in the face of continued propafenone therapy.
Drug-induced lupus (Systemic Lupus Erythematosus, SLE) is a clinical picture simulating systemic lupus erythematosus that can be produced by certain drugs, including hydralazine 2 and procainamide 3. It is characterized by symptoms such as arthralgia, pleural or abdominal pain, and sometimes arthritis, pleural effusion, pericarditis, fever, chills, myalgia, and possibly related hematologic or skin lesions. Positive ANA titers may also be present, as seen with propafenone 4. Discontinuation of the offending drug usually leads to regression of symptoms.
From the Research
Definition and Characteristics of Drug-Induced Lupus
- Drug-induced lupus is a syndrome resembling mild systemic lupus erythematosus (SLE) that can complicate treatment with certain medications 5.
- It is characterized by arthralgia, myalgia, pleurisy, rashes, and fever in association with antinuclear antibodies in the serum 5.
- The syndrome is often milder than idiopathic SLE, with rare occurrences of serious features like nephritis and cerebral disease 5, 6.
Drugs Associated with Drug-Induced Lupus
- High-risk drugs include hydralazine, procainamide, and isoniazid 6, 7.
- Other drugs associated with drug-induced lupus are chlorpromazine, methyldopa, penicillamine, quinidine, and sulfasalazine 5.
- Whole drug groups implicated include anticonvulsants, beta-blockers, sulfonamides, and biological agents like interferons and anti-TNFα agents 5, 6, 8.
- Anti-TNFα therapies have been associated with a "lupus-like" syndrome, which is clinically distinct from classical drug-induced lupus 6, 8.
Diagnosis and Treatment
- There are currently no standard diagnostic criteria for drug-induced lupus 6, 8.
- Diagnosis requires identification of a temporal relationship between drug administration and symptom development, and resolution of symptoms after cessation of the drug 9, 7.
- Clinical resolution generally occurs after withdrawal of the offending agent, making early diagnosis and vigilance critical 5, 9, 7.